Rapid efflux of lactate from cerebral cortex during K+-induced spreading cortical depression

Rapid transport of lactate from activated brain regions to blood, perhaps r eflecting enhanced metabolite trafficking, would prevent local trapping of labeled metabolites of [6-C-14]glucose and cause underestimation of calcula ted CMR-(glc). Because the identities of glucose metabolites lost from acti vated structures and major routes of their removal are not known, arteriove nous differences across brains of conscious normoxic rats for derivatives o f [6-C-14]glucose were determined under steady-state conditions in blood du ring K+-induced spreading cortical depression. Lactate was identified as th e major labeled product lost from brain. Its entry to blood was detected wi thin 2 minutes after a pulse of [6-C-14]glucose, and it accounted for 96% o f the C-14 lost from brain within approximately 8 minutes. Lactate efflux c orresponded to 20% of glucose influx, but accounted for only half the magni tude of underestimation of CMRglc, when [C-14]glucose is the tracer, sugges ting extensive [C-14]lactate trafficking within brain. [C-14]Lactate spread ing within brain is consistent with (1) relatively uniform pattern labeling of K+-treated cerebral cortex by [6-C-14]glucose contrasting heterogeneous labeling by [C-14]deoxyglucose, and(2)transport of C-14-labeled lactate an d inulin up to 1.5 and 2.4 min, respectively, within 10 minutes. Thus, newl y synthesized lactate exported from activated cells rapidly flows to blood and probably other brain structures.